4.6 Article

Cardioprotective Properties of Omentin-1 in Type 2 Diabetes: Evidence from Clinical and In Vitro Studies

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PLOS ONE
卷 8, 期 3, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0059697

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资金

  1. Federal Ministry of Health
  2. Ministry of Innovation, Science, Research and Technology of the German State of North Rhine Westphalia
  3. Commission of the European Communities [HEALTH F2-2008-201100]
  4. German Centre for Diabetes Research (Deutsches Zentrum fur Diabetesforschung, DZD)
  5. Eli Lilly, The Netherlands
  6. Medtronic
  7. Boston Scientific
  8. Biotronik
  9. St. Jude Medicial
  10. BMS Medical Imaging
  11. Edwards Lifesciences
  12. GE Healthcare
  13. Amylin Pharmaceuticals Inc
  14. Novo Nordisk
  15. Merck
  16. Sharp
  17. Dohme
  18. Sanofi

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Context: Adipokines are linked to the development of cardiovascular dysfunction in type 2 diabetes (DM2). In DM2-patients, circulating levels of omentin-1, an adipokine preferentially expressed in epicardial adipose tissue, are decreased. This study investigated whether omentin-1 has a cardioprotective function. Methods: Omentin-1 levels in plasma and cardiac fat depots were determined in DM2-patients versus controls. Moreover, the relation between omentin-1 levels and cardiac function was examined in men with uncomplicated DM2. Finally, we determined whether omentin-1 could reverse the induction of cardiomyocyte dysfunction by conditioned media derived from epicardial adipose tissue from patients with DM2. Results: Omentin-1 was highly expressed and secreted by epicardial adipose tissue, and reduced in DM2. Circulating omentin-1 levels were lower in DM2 versus controls, and positively correlated with the diastolic parameters early peak filling rate, early deceleration peak and early deceleration mean (all P<0.05). The improved diastolic function following pioglitazone treatment associated with increases in omentin-1 levels (P<0.05). In vitro, exposure of cardiomyocytes to conditioned media derived from epicardial adipose tissue from patients with DM2 induced contractile dysfunction and insulin resistance, which was prevented by the addition of recombinant omentin. Conclusion: These data identify omentin-1 as a cardioprotective adipokine, and indicate that decreases in omentin-1 levels could contribute to the induction of cardiovascular dysfunction in DM2.

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